Edith Hamel, PhD

Edith Hamel, PhD
Contact Information
Email address: 
edith.hamel [at] mcgill.ca

Edith Hamel's research focuses on the interactions between neurons, astrocytes and microvessels that assure a proper blood supply to activated brain areas, a phenomenon commonly referred to “neurovascular coupling.” These interactions are at the basis of several brain-imaging techniques that use hemodynamic signals to map changes in brain activity under physiological and pathological conditions. The underlying cellular mechanisms and chemical mediators of these signals are poorly understood. This is important because the dysfunction of specific populations of cells might have dramatic repercussions on the regulation of local blood flow. Moreover, several neurological conditions are associated with a cerebrovascular pathology and impaired neurovascular coupling responses.

The Hamel lab uses various in vivo techniques such as optogenetic or electrical stimulation of selected brain neurons, imaging of optical intrinsic signals (OIS), laser speckle contrast imaging (LSCI) and laser Doppler flowmetry (LDF) to record changes in neuronal and hemodynamic responses. These are combined with anatomical identification of the neuronal networks involved, and pharmacological manipulations to identify the mediators of the neuronal and vascular responses or how these are modulated during different brain states. The Hamel lab aims at deciphering how brain neurons control local cerebral perfusion and how this relationship is altered in pathologies like Alzheimer’s disease and vascular cognitive impairment and dementia. The lab is testing the hypothesis that rescuing cerebrovascular function will have a positive outcome on the onset and progression of cognitive decline in these two most frequent types of dementia in the elderly. Her group hypothesizes that it might be possible, at specific time points in the disease, to rescue or delay the manifestation of cognitive alterations with drugs originally designed to treat cardiovascular diseases, but that also exert pleiotropic effects on various cell types in the brain. The research team is asking whether cerebrovascular and cognitive recovery are interrelated or independent from each other. Ultimately, she and her research group aim to identify new therapeutic targets or drugs to preserve cerebral perfusion and rescue of neuronal function.

Selected publications: 

Ongali B, Aboulkassim T, Tong X-K, Nicolakakis N, Rosa-Neto P, Lecrux C, Imboden H and Hamel E. (2014) Losartan rescues cerebrovascular dysfunctions and memory deficits in Alzheimer’s disease mice. Neurobiol Dis, 68: 126-136.

Papadopoulos P, Tong X-K, Hamel E. (2014) Selective benefits of simvastatin in bitransgenic APPSwe,Ind/TGF-b1 mice. Neurobiol Aging 35(1): 203-212.

Tong X-K and Hamel E. (2015) Simvastatin restored the vascular reactivity, endothelial function and reduced string vessel pathology in a mouse model of cerebrovascular disease. J Cereb Blood Flow Metab, 35(3):512-520.

Lacroix A, Toussay X, Anenberg E, Lecrux C, Karagiannis A, Plaisier F, Chausson P, Jarlier F, Burgess SA, Hillman EMC, Murphy TH, Hamel E and Cauli B. (2015) Prostaglandin E2 produced by pyramidal neurons underpins neurovascular coupling. J Neurosci, 35(34):11791-11810.

Lecrux C, Sandoe CH, Neupane S, Krop P, Toussay X, Tong X-K, Shmuel A, Hamel E. (2017). Altered brain states impact neuronal correlates of hemodynamic signals, J Neurosci, 37(6):1518-1531.

Badhwar A, Brown R, Stanimirovic DB, Haqqani AS, Hamel E (2017). Proteomic differences in brain vessels of Alzheimer’s disease mice: normalization by PPARγ agonist pioglitazone. J Cereb Blood Flow Metab 37 (3): 1120-1136.

Royea J, Zhang L, Tong X-K, Hamel E. (2017) The angiotensin IV receptor: a potential target for cerebrovascular and cognitive rescue in a mouse model of Alzheimer's disease. J Neurosci 37(32):5562-5573.

Research areas: 
Neural Circuits

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